Effects of Oxygen and Antioxidants on the Mitochondrial Ca-Retention Capacity

Guidoux, R.; Lambelet, Pierre; Phoenix, Joanne

doi:10.1006/abbi.1993.1491

Cited by 8 publications

(4 citation statements)

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“…This conclusion is supported by the high amount of carbonyls bound to proteins (8.36 _+ 0.93 nmol/mg compared to 3.59 nmol/mg _+ 0.27 nmol/mg of the control, n = 5) which are accepted to be a sensitive marker of oxidative protein modifications (24,33). The short time of anoxia which is sufficient to cause the functional damage of the mitochondria in our experiments differs from larger anoxic periods used by others (31,32). One reason for this apparent contradiction could be the incubation temperature.…”

Section: Discussionmentioning

confidence: 48%

“…Reoxygenation stimulated the permeability transition rather by changing the redox energy than by producing ROS. It was concluded that ROS favour pore opening but were not necessarily needed to initiate permeability transition during anoxia-reoxygenation at high calcium load (32). In contradiction, ROS are definitely required to cause permeability transition at lower calcium concentrations as was demonstrated by blocking pore opening using catalase (15).…”

Section: Discussionmentioning

confidence: 99%

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Micromolar calcium prevents isolated rat liver mitochondria form anoxia‐reoxygenation injury

et al. 1997

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Rat liver mitochondria were exposed to extramitochondrial free calcium between 0 and 5 μM and/or 5 minutes of anoxia followed by 10 minutes of reoxygenation. At concentrations higher than 4 μM, the membrane potential collapsed indicating the permeability transition of the mitochondrial membrane. Anoxia‐reoxygenation shifted this transition to lower calcium concentrations. Anoxia‐reoxygenation alone resulted in the decrease of ADP stimulated respiration down to about 40 % of its initial value. Between 1 and 2 μM, a protective effect in terms of respiration and oxidative protein modification was found. It is concluced that calcium may suppress the formation of reactive oxygen species during anoxia‐reoxygenation before permeability transition occurs.

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Section: Discussionmentioning

confidence: 48%

Section: Discussionmentioning

confidence: 99%

Micromolar calcium prevents isolated rat liver mitochondria form anoxia‐reoxygenation injury

et al. 1997

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“…Vitamin E can block the glycation of proteins by inhibiting MDA formation [38]. However, some reports suggest that the Ca 2 + -releasing and/or -retaining effects of alpha-tocopherol may be independent of pro-and/or antioxidant activities [45].…”

Section: Discussionmentioning

confidence: 99%

In vivo treatment with stobadine prevents lipid peroxidation, protein glycation and calcium overload but does not ameliorate Ca2+-ATPase activity in heart and liver of streptozotocin-diabetic rats: comparison with vitamin E

Pekiner

Ulusu

Daş-Evcimen

et al. 2002

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Hyperglycemia leads to excess production of reactive oxygen species (ROS), lipid peroxidation and protein glycation that may impair cellular calcium homeostasis and results in calcium sequestration and dysfunction in diabetic tissues. Stobadine (ST) is a pyridoindole antioxidant has been postulated as a new cardio- and neuroprotectant. This study was undertaken to test the hypothesis that the treatment with ST inhibits calcium accumulation, reduces lipid peroxidation and protein glycation and can change Ca2+,Mg2+-ATPase activity in diabetic animals. The effects of vitamin E treatment were also evaluated and compared with the effects of combined treatment with ST. Diabetes was induced by streptozotocin (STZ, 55 mg/kg i.p.). Some of diabetic rats and their age-matched controls were treated orally with a low dose of ST (24.7 mg/kg/day), vitamin E (400-500 IU/kg/day) or ST plus vitamin E for 10 weeks. ST and vitamin E separately produced, in a similar degree, reduction in diabetes-induced hyperglycemia. Each antioxidant alone significantly lowered the levels of plasma lipid peroxidation, cardiac and hepatic protein glycation in diabetic rats but vitamin E treatment was found to be more effective than ST treatment alone. Diabetes-induced increase in plasma triacylglycerol levels was not significantly altered by vitamin E treatment but markedly reduced by ST alone. The treatment with each antioxidant completely prevented calcium accumulation in diabetic heart and liver. Microsomal Ca2+,Mg2+-ATPase activity significantly decreased in both tissues of untreated diabetic rats. ST alone significantly increased microsomal Ca2+,Mg2+-ATPase activity in the heart of normal rats. However, neither treatment with ST nor vitamin E alone, nor their combination did change cardiac Ca2+,Mg2+-ATPase activity in diabetic heart. In normal rats, neither antioxidant had a significant effect on hepatic Ca2+,Mg2+-ATPase activity. Hepatic Ca2+,Mg2+-ATPase activity of diabetic rats was not changed by single treatment with ST, while vitamin E alone completely prevented diabetes-induced inhibition in microsomal Ca2+,Mg2+-ATPase activity in liver. Combined treatment with ST and vitamin E provided more benefits in the reduction of hyperglycemia and lipid peroxidation in diabetic animals. This study describes potential mechanisms on cellular effects of ST in the presence of diabetes-induced hyperglycemia that may delay or inhibit the development of diabetic complications. The use of ST together with vitamin E can better control hyperglycemia-induced oxidative stress.

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“…5 Numerous studies with isolated mitochondria have shown that under conditions of oxidative stress some antioxidants, like butylated hydroxytoluene (BHT), αtocopherol, and retinol, can prevent mitochondrial PT and hence maintain the ability of mitochondria to retain Ca 2+ under pathological circumstances. [6][7][8] However, in spite of the increasing number of publications on the ability of antioxidants to prevent mitochondrial PT, some aspects of this problem are still equivocal. In particular, the widely-used potent antioxidant BHT was shown to prevent mitochondrial damage induced not…”

Section: Introductionmentioning

confidence: 99%

Substrate-dependent effect of phenolic antioxidants on Ca²⁺accumulation by rat liver mitochondria

Ryan¹,

Gogvadze

1999

Redox Report

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The effect of different phenolic antioxidants on mitochondrial Ca2+ capacity (maximum amount of Ca2+ mitochondria can accumulate) was studied. Butylated hydroxytoluene substantially enhanced the Ca2+ capacity in mitochondria oxidizing succinate, butylated hydroxyanisole had a moderate effect while 2,5-di-(t-butyl)- 1,4 benzohydroquinone did not affect Ca2+ capacity at all. The analysis of Ca2+ accumulation in mitochondria oxidizing succinate in the presence of 2,5-di-(t-butyl)-1,4 benzohydroquinone revealed inhibition of the rate of Ca2+ accumulation. This effect was absent when ATP hydrolysis or NAD+-dependent substrate oxidation supported Ca2+ transport. Direct measurements of oxygen consumption revealed the concentration-dependent inhibition of succinate oxidation by increasing concentrations of 2,5-di-(t-butyl)- 1,4 benzohydroquinone. When succinate was substituted by NAD+-dependent respiratory substrates, the Ca2+ capacity of mitochondria with 2,5-di-(t-butyl)-1,4 benzohydroquinone was even higher than in the presence of butylated hydroxytoluene.

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Effects of Oxygen and Antioxidants on the Mitochondrial Ca-Retention Capacity

Cited by 8 publications

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Micromolar calcium prevents isolated rat liver mitochondria form anoxia‐reoxygenation injury

Micromolar calcium prevents isolated rat liver mitochondria form anoxia‐reoxygenation injury

In vivo treatment with stobadine prevents lipid peroxidation, protein glycation and calcium overload but does not ameliorate Ca2+-ATPase activity in heart and liver of streptozotocin-diabetic rats: comparison with vitamin E

Substrate-dependent effect of phenolic antioxidants on Ca²⁺accumulation by rat liver mitochondria

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Effects of Oxygen and Antioxidants on the Mitochondrial Ca-Retention Capacity

Cited by 8 publications

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Micromolar calcium prevents isolated rat liver mitochondria form anoxia‐reoxygenation injury

Micromolar calcium prevents isolated rat liver mitochondria form anoxia‐reoxygenation injury

In vivo treatment with stobadine prevents lipid peroxidation, protein glycation and calcium overload but does not ameliorate Ca2+-ATPase activity in heart and liver of streptozotocin-diabetic rats: comparison with vitamin E

Substrate-dependent effect of phenolic antioxidants on Ca2+accumulation by rat liver mitochondria

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Substrate-dependent effect of phenolic antioxidants on Ca²⁺accumulation by rat liver mitochondria